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Neonate > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

complete or partial absences of a structure caused by environmental or genetic factors

A

malformation

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2
Q

due to mechanical forces that mold a previously normal part of the fetus over a prolonged period
-often MSK and reversible

A

deformations

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3
Q

destructive processes which result in morphological alterations of already formed structures

A

disruption

ex. limb defects caused by amniotic bands

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4
Q

groups of anomalies occuring together which have a common cause*

A

syndromes

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5
Q

groups of anomalies that often occur together more often than chance alone would allow but whose cause has not yet been determined

A

associations

ex. CHARGE association

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6
Q

agents, generally chemical, radioactive or infectious which can produce birth defects. These are especially destructive when exposure occurs during the period of organogenesis

A

teratogens

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7
Q

____ the most common cause of low birth weight babies in the developing world

A

malnutrition

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8
Q

macrosomia

A

excessive birth weight

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9
Q

insulin acts as a powerful growth hormone in the fetus, causing

A

macrosomia

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10
Q

excessive insulin results in risk of ___

A

hyperglycemia in the newborn period

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11
Q

Describe insulin and glucose and how it relates to the fetus

A

insulin does not cross the placenta but glucose does. The fetus secretes increased level of insulin to regulate hyperglycemia

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12
Q

glucose is more teratogenic to the fetus when

A

1st trimester

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13
Q

hyperthyroidism in mom (ie. Grave’s disease) affects the baby how?

A
  • thyroid hormone can cross the placenta slowly

- can cause growth retardation or prematurity in newborns

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14
Q

How does hypothyroidism affect baby

A

can cause decreased IQ or small stature

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15
Q

Pre-eclamplsia

A

HTN that generally begins in 3rd trimester and is associated with edema (maternal) and proteinuria

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16
Q

Eclamplsia

A

HTN, edema, proteinuria and maternal seizures

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17
Q

HELLP

A

severe form of eclampsia with associated Hemolysis, Elevated Liver, Low Platelets

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18
Q

How does HTN in mom affect baby?

A

related to insufficient blood supply to placenta bc of vasocontriction

  • IUGR (intrauterine growth restriction)
  • premature delivery
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19
Q

pregnancy risks in extreme younth

A
  • pregnancy induced HTN

- prematurity

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20
Q

pregnancy risks with advanced maternal age

A
  • Down syndrome (or other chromosomal non-disjunctions)
  • increased fetal loss
  • inadequate milk supply
  • increased risk of pre-eclampsia and HTN
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21
Q

Taking Dilantin (phenytoin) during pregnancy is associated w/

A

fetal hydantoin syndrome- consisiting of cleft lip and palate as well as mental retardation

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22
Q

Taking Valproic acid during pregnancy is associated w/

A

neural tube defects (eg. spina bifida)

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23
Q

Taking Keppra during pregnancy

A

has limited study but shows no teratogenicity

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24
Q

taking Lamictal during pregnancy shows

A

0.9% (8.9/1000) incidence of cleft lip +/- palate

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25
Q

taking Lithium during pregancy is associated w/

A

risk of Ebstein abnormality (displacement of TV into RV)

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26
Q

taking Phenothiazines (older anti-psychotic med ex. Haldol and Thorazine) during pregancy is associated w/

A

no known teratogenic effects but had disagreeable side-effects for adult pt.

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27
Q

what antidepressants are ok to take during pregnancy?

A
  1. Tricyclics (ex. amitriptyline and nortriptyline)
  2. SSRI (ex. Celexa, Prozac, Zoloft)
  3. Wellbutrin

**avoid Paxil- doubles risk of septal defects in fetus

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28
Q

Xrays during pregnancy are known to cause

A

microcephaly, spina bifida, celft palate, limb defects

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29
Q

most common cause of IUGR in developed countries an its mechanism

A

Tobacco!

  • direct teratogen
  • vasoconstriction
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30
Q

tobacco increases risk of (4)

A

spontaneous abortion, prematurity, perinatal mortality, and SIDS

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31
Q

most prevalent problem for cocaine babies is

A

prematurity
(stimulates uterine contractions, coupled with decreased blood flow causes premature labor, premature rupture of membranes and attendant complications )

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32
Q

most prevalent problem for amphetamine babies is

A

neglect

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33
Q

3 major components of Fetal alcohol syndrome

A
  1. prenatal and postnatal growth deficiencies
  2. Microcephaly w/ cognitive impairment
  3. Typical facies (short palpebral fissure, indistinct philtrum, thin upper lip)
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34
Q

When do most malformations originate and give an example

A

during the period of organogenesis, the 3rd to 8th weeks of gestation
-ex. CHD, tetralogy of fallot

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35
Q

components of tetralogy of fallot

A
  1. VSD
  2. pulmonic stenosis or infundibular stenosis
  3. dextroposition of the aorta so taht it overrides the ventricular septum and receives venous and arterial blood
  4. RVH
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36
Q

when do deformations occur and give an example

A

during fetal period (after 9 weeks)

ex. clubfoot

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37
Q

what pregnancy risks to obese women have

A
  1. diabetes
  2. pre-eclampsia
  3. higher likelihood of c-section and more difficulty healing
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38
Q

obesity is considered BMI > __

A

BMI > 31

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39
Q

compare birth weights of obese women compared to non-obese women

A
  • equal weights in comparison

- BUT have 30% more fat, at expense of lean body mass

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40
Q

malnutrition can cause

A
  • life long immunodeficiency
  • short stature
  • congnitive impairment
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41
Q

a B-complex vitamin which can reduce the risk of neural tube defects by 70%

A

folic acid

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42
Q

when should you start takign folic acid

A

2 months prior to conception

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43
Q

what vitamins should mom take during pregnancy

A
  1. folic acid
  2. calcium
  3. iron
  4. Vit. D
  5. Vit. A
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44
Q

for bones, teeth, muscle, CNS

A

calcium

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45
Q

for development of blood cells, CNS

A

iron

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46
Q

for bones and teeth and improved immunity

A

Vit. D

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47
Q

important for development of eyes

A

Vit. A

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48
Q

excess Vit. A and isotretinoin can cause

A 
major malformations
(isotretinoin= accutane)
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49
Q

Effects of different types of DM (pregestational, gestational, Type I, Type II)

A

all have same effect on fetus

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50
Q

excessive glucose can cause

A
  • caudal regression syndromes

- malformations of hips and legs

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51
Q

extreme youth is defined as

A

less than 15 y/o

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52
Q

advanced maternal age is defined as

A

greater than 35 y/o

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53
Q

effects of general anesthesia to a pregnant woman

A

it is not teratogenic

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54
Q

can surgery be performed on MOC during pregnancy

A

yes

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55
Q

how does marijuana affect the fetus

A
  1. measurable cognitive impairment
  2. mild neurologic abnormalities such as jitteriness, irritability in newborn period
  3. IUGR
    * side effects are controversial
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56
Q

Prescription: fentanyl, oxycodone, methadone, morphine

Non-prescription: heroin

A

opiates

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57
Q

effects of opiates on the baby

A
  • physical abnormalities are rare
  • acute intoxication at delivery can cause respiratory suppression
  • born dependent and exhibit signs of withdrawl
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58
Q

treat withdrawl symptoms of a baby with

A

methadone taper

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59
Q

Effects are result of inhibition of re-uptake of epinepherine, norepinepherine, dopamine and serotonin neurotransmitters by sympathetic nerve endings, thus increasing concentration of neurotransmitters

A

cocaine

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60
Q

dopamine can casue

A

euphoria and addiction

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61
Q

Norepinepherine and epinepherine are neurotransmitters which cause

A
  1. vasoconstriction
  2. hypertension
  3. tachycardia
  4. diminshed blood flow
  5. fetal hypoxia
  6. IUGR
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62
Q

causes of IUGR

A
  1. malnutrition
  2. tobacco
  3. Marijuana
  4. Cocaine
  5. Ampetamines
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63
Q

cocain can cause

A
  • microcephaly,
  • IUGR,
  • local defects to eyes, limbs, heart and urogenital system, attributable to ischemic events in utero
  • hypoxia
  • tachycardia
  • vasoconstriction
  • intoxication at birth
  • long-term: cognitive and behavioral problems
  • **no motor deficits
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64
Q

synthetic chemicals with properties similar to cocaine but with longer half-life

A

amphetamines

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65
Q

amphetamines can cause

A
  • neglect
  • -IUGR,
  • microcephaly*
  • cleft lip* and
  • palate* w/o specific syndrome
  • neurobehaviors (ADHD and aggression)
  • *** no intellectual deficits defined at this time
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66
Q

alcohol can cause

A
  • neurodevelopmental problems (ADHD, communication and socialization problems)
  • FAS
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67
Q

how much alcohol is needed to cause FAS?

A

unknown, therefore recommend abstention during pregnancy

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68
Q

what does APGAR stand for and how is it scored?

A 
A-appearance (color) -2
P- pulse (HR)- 2
G- Grimace (reflex irritability/ response to stimuli)- 2
A- activity (tone)- 2
R- respiratory (RR)- 2

Total of 10
* Colorado babys never get 10

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69
Q

how to you check for grimace

A

rub babe’s back or feet to stimulate a cry

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70
Q

Neonatal circulation shunts

A
  1. ductus arteriosus
  2. Umbilical arteries
  3. Umbilical vein
  4. Ductus vensosus
  5. Foramen ovale
  6. Functional shunt
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71
Q

shunt between pulmonary artery & aorta

A

Ductus arteriosus

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72
Q

branches of common iliac arteries- to placenta

A

umbilical arteries

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73
Q

from placenta to liver or DV

A

umbilical vein

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74
Q

option to bypass liver, direct to IVC

A

ductus venosus

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75
Q

interatrial shunt

A

Foramen ovale

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76
Q

increased pulmonary pressure (shunt)

A

functional shunt

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77
Q

no valves so has bidirectional flow (high to low pressure)

carries 40% of cardiac output

A

DA

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78
Q

what filters out impurities of the blood for the baby

A

placenta

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79
Q

describe the pressure system for system vs lungs in a fetus and adult

A

fetus: higher pressure in lungs than systemic circulation (blood bypasses lungs via functional shunt and DA)
adult: higher systemic pressure than lungs

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80
Q

how much blood goes to the lungs in the fetus

A

10-30%

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81
Q

where does most of the oxygenated blood go in the heart?

A

through the foramen ovale

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82
Q

of any gas is a measurement, in essence, of how much gas there is in any environment

A

partial pressure

83
Q

what does a pulse ox measure

A

% of blood carrying oxygen

84
Q

what is the % saturation of oxygen air

A

21% regardless of altitude

- the number of molecules of oxygen are fewer as altitude increases

85
Q

normal oxygen saturation after transition period

A

> 95%

86
Q

What happens to the babys pO2 after the baby starts to breathe air

A

increase in pO2 in blood

87
Q

Increase in pO2 in blood when baby starts to breathe air causes:

A
  1. Dilatation of vessels in pulmonary bed drops pulmonary pressures; therefore, right sided pressures become lower than left (functional shunt gone)
  2. Constriction (Closure) of ductus arteriosus
88
Q

what does cutting off the umbilical circulation cause during the transition period

A
  1. systemic pressure to increase

2. therefore, increased volume elsewhere

89
Q

in the fetus, what side of the heart has higher pressure

A

right sided pressure is always higher

90
Q

pressure effect of having LA pressures greater than RA pressure causes

A

Foramen ovale to close

91
Q

why does the ductus venosus close

A

bc there is no longer flow through it

92
Q

DA normally closes within

A

48 hrs

93
Q

DA closes by

A
  1. increase pO2 (DA constricts)

2. Decrease in prostaglandins

94
Q

Umbilical vein and arteries close becasue

A

blood supply is cut off

95
Q

DV closes because

A

blood supply is cut off

96
Q

Foramen ovale closes because

A

there is a change in pressure to LA>RA

97
Q
  • Time from onset of ventricular contraction until closure of aortic and pulmonary valves
  • Begins with first heart sound- closure of tricuspid and mitral valves
A

systole

98
Q
  • Time of filling of chambers

- Time between second and first heart sounds

A

Diastole

99
Q

most common congenital malformation in newborns

A

congenital heart disease
-at least 35 variations
1% in general population

100
Q

Recurrence of CHD is greater in

A
  1. those with siblings that have CHD, 1-3% recurrence
  2. those whose mom has CHD, 15% recurrence
    * *not necessarily the same defect
101
Q

Critical congenital heart disease requires intervention within

A

first 28 days

102
Q

serious congential heart disease requires intervention within

A

1st year

103
Q

causes/risk factors of CHD

A
  1. sibling or parent has CHD
  2. genetic abnormalities
  3. Maternal conditions (ex. DM , alcohol use)
104
Q

___% of childen with Down Syndrome also have CHD

A

40%

105
Q

How does congenital heart disease present in a newborn?

A
  • Cyanosis
  • Heart failure (or its extreme, shock)
  • Cardiac murmur

*varies on nature and severity of defect and Alterations in cardiovascular physiology in the transitional period

106
Q

Two possible causes of central cyanosis

A
  1. Decreased pulmonary blood flow causing a shunt

2. Mixing of oxygenated and deoxygenated blood in heart

107
Q

cyanosis is typically not recognized until pulse ox is in ___

A

low 80s

108
Q

Most babies that are cyanotic is due to ____

A

pulmonary origin

109
Q

DDX of central cyanosis

A
  1. primary lung disease such as pneumonia, RDS, meconium aspiritation, etc.
  2. airway obstruction
  3. Hypoventilation (drug induced or neurological)
  4. polycythemia
  5. Congential heart disease
110
Q

Origin of cyanosis?

  • Labored breathing
  • Improves with 100% oxygen supplementation
  • Cyanosis often improves with crying
A

Pulmonary

111
Q

Origin of cyanosis?

  • Non-labored respirations
  • No or minimal response to 100% oxygen
  • Cyanosis worsens or doesn’t improve with crying
A

Cardiac

112
Q

Most sensitive tool for differentiating between primary pulmonary and cyanotic congenital heart disease

A

hyperoxitest

113
Q

how do you perform a hyperoxitest?

A

measure pO2 by blood gas or pulse on in room air, then check pO2 on 100% oxygen after 10 min, note pulse ox/blood gas again,
**A patient with primary pulmonary disease will usually dramatically increase saturation when given oxygen
Cardiac etiology will have no improvement

114
Q

signs and symptoms of congestive heart failure

A
  1. increased LA pressure causes congestion and pulmonary edema
  2. tachypnea
  3. tachycardia
  4. Hepatomegaly
  5. Sweating and feeding difficulties
115
Q

Descriptors of cardiac murmur

A
  1. Intensity
  2. Timing in systole or diastole
  3. Quality
  4. Location
  5. Transmission
116
Q

Grade Intensity on a 6 point scale

A
  1. Barely audible
  2. Soft but easily audible
  3. Moderately loud, but without thrill
    Louder and associated with a thrill
  4. Audible with stethoscope barely on chest
  5. Audible with stethoscope off the chest (usually a mechanical valve)
117
Q

what does it mean if the murmur is vibratory or muscial

A

likely innocent

118
Q

a murmur that is high-pitched and blowing/or coarse indicates

A

VSD

119
Q

grating murmur indicates

A

aortic stenosis (AS) or pulmonic stensosis (PS)

120
Q

you can distinctly hear S1, closing of the tricuspid and mitral valves

A

ejection murmur

aka “crescendo-decrescendo

121
Q

Caused by flow through stenotic or deformed semilunar valve

A

ejection murmur

122
Q

you can’t separate the murmur from S1

A

regurgitant murmur

123
Q

caused by flow of blood from a chamber that is at higher pressure to one of lower pressure eg. VSD

A

regurgitant type murmur

124
Q

Most common benign murmurs

A
  1. pulmonic flow murmur aka peripheral pulmonic stenosis or PPS** (most common)
  2. Physiologic ductus arteriosus
  3. Tricuspid jet
125
Q

Loudest at left upper sternal border but radiates throughout the precordium and to the axillae and back
-Usually Grade I-II/VI

A

pulmonary flow murmur or PPS

126
Q

Caused by relatively hypoplastic pulmonary arteries- normally formed but underused in fetal life
(Hearing the turbulence against the pulmonary vessels)

A

pulmonary flow murmur or PPS

127
Q

Systolic murmur heard at ULSB and below left clavicle

- Usually Grade I-II/VI

A

physiologic ductus arteriosus murmur

*usually only heard on 1st day of life bc ductus closes off by 2nd day

128
Q

when the PVR is low enough to function but still high enough to cause a little bit of blood to squirt through and cause a murmur

A

tricupsid jet murmur

129
Q

What is the cause of pathologic murmurs that occur at birth

A

those of stenotic lesions (isolated)

*not affected by changes in pulmonary vascular resistance

130
Q

what is the cause of pathologic murmurs that present later

A

murmurs of left to right shunts (like VSD) depend on reduction in pulmonary vascular resistance

131
Q

Further evalution of a murmur

A 
Fetal echocardiogram
History- maternal medical, pregnancy
Physical exam
Signs of CHF, Cyanosis, murmur
4-point blood pressures (all extremities)
Pulse oximetry study
Chest x-ray
Electrocardiogram
Echocardiogram
132
Q

benefits of fetal echos

A
  • 60% diagnosed before birth

- most severe diagoses can be determined (except: coarctation, small VSD, ASD)

133
Q

when are the most accurate fetal echos done

A

at 18- 20 weeks

134
Q

BP is done to look for __ in a newborn

A

coarctation of the aorta

135
Q

___mm Hg difference between right arm and legs is significant for coarctation

A

10 mmHg

136
Q

Select the right size blood pressure cuff

A
  • width should be 125%-155% of the diameter of the limb

- length should be long enough to completely encircle the limb

137
Q

cyanosis does not show up until

A
138
Q

for a pulse ox reading to be considered accurate what needs to occur

A

HR on monitor match manual HR and regular respiratory pattern on screen

139
Q

______ baby looks more cyanotic than an anemic one at the same saturation

A

polycythemic baby

140
Q

Enlarged heart and pulmonary edema (diffusely opaque lung fields) on chest xray are signs of

A

CHF

141
Q

dark lung fields on chest xray indicates

A

decreased pulmonary vascular flow

142
Q

Boot-shaped heart xray

A

Fallot Tetralogy

143
Q

Egg on a string chest xray

A

Transposition of great vessels

144
Q

primary diagnostic tool for anatomic definition of congenital heart lesion

A

echocardiogram

costs $3000

145
Q

Types of neonatal CHD

A
  1. Obstruction to the flow of blood in the heart or great vessels caused by underdevelopment of structures
  2. Blood flows in abnormal patterns
146
Q

example of obstruction CHD

A
  • Valvular atresia/stenosis
  • Hypoplastic left or right heart syndromes
  • Coarctation of the aorta/interrupted aortic arch
147
Q

From right to left (blue mixes with red)-leads to

A

cyanosis

148
Q

From left to right (red mixes with blue)-leads to

A

CHF

ex. VSD

149
Q

pressure from RA to LA presents as

A

cyanotic lesion

ex. PFO

150
Q

most common cyanotic lesions in newborn (7)

A
  1. Transposition of the Great Vessels
  2. Truncus arteriosus
  3. Tricuspid atresia
  4. Tetralogy of Fallot
  5. Total anomalous pulmonary venous return (TAPVR)
  6. Pulmonary atresia
  7. Hypoplastic left heart
151
Q

most common acyanotic lesions in newborn (5)

A
  1. Patent ductus arteriosus (PDA)
  2. Large septal defects (VSD, ASD)
  3. Critical aortic stenosis
  4. Coarctation of the Aorta
  5. Hypoplastic left heart
152
Q

what causes a drop in prostaglandins

A

loss of placenta

153
Q

direction of blood flow in fetus

A

R–> L

154
Q

pathologic direction of blood flow

A

L–> R

155
Q

15% of infants with ____ have other cardiac defects

A

PDA

*associated defects may cause the ductus to close more slowly (ex. coarctation of the aorta)

156
Q

Most frequent disorder in premature newborns

A

PDA

patent ductus arteriosus

157
Q

How is PDA treated

A

Treated with indomethacin (in preterm babies) or surgical ligation

158
Q

what could happen if mother takes advil or NSAID during pregnancy

A

could close off DA

**Take tylenol

159
Q

most common congenital heart disease

A

VSD

160
Q

The magnitude of the Left to Right shunt is determined by

A

the size of the defect and the pulmonary vascular resistance (PVR).

161
Q

PVR is highest when

A

first days of life, gradually falls over weeks

162
Q

VSD blood flow in fetus

A

R –> L

163
Q

VDS blood flow in newborn

A

L —> R

164
Q

how to treat VSD

A
  • 50% to 75% of small VSDs will close spontaneously
  • try diuretics or digoxin (medications of CHF)
  • large ones get closed surgically w/ patch (via cardiac catheterization and placement of an occluder)
165
Q

Longterm risk of untreated VSD

A

development of pulmonary vascular disease (hypertension) with continued pulmonary overcirculation
aka. Eisenmenger’s complex

166
Q

Fixed pulmonary pressures that are non-reversible due to chronic VSD (has a lof of cardiac output on right side)

A

Eisenmenger’s complex

167
Q

Can occur anywhere, but usually juxtaductal and presents when DA closes

A

Coarctation of aorta

168
Q

coarctation of aorta often has associated

A

bicupsid aortic valvee (50%)

169
Q

causes Impaired LV output, decreased pulses below, differential BP and CHF/ shock/ renal failure are late findings

A

coarctation

170
Q

CHD frequently in Turner Syndrome

A

coarctation

171
Q

When do a baby’s symptoms of coarctation occur

A

after DA closes and prostaglandins are gone

172
Q

tachypnea, appears in shock, no femoral pulse, poor peripheral perfusion (looks septic- but don’t have femoral pulses!)

A

early presenting coarctation of aorta

**typically has some other shunt lesion

173
Q

treatment of early presenting coarctations

A

Prostaglandins aka PGE1 (life-saving but temporary fix)

-requires surgery once baby is stable (cath and balloon dilation)

174
Q

side effects of prostaglandins

A

apnea

175
Q

Average age of presentation is 5 years

-Presents with hypertension, easy fatigue in legs

A

late presenting coarctation

**great collateral circulation because no other shunt

176
Q

treatment of late presenting coarctation

A

non-emergent

-requires surgery (cath and balloon dilation)

177
Q

may open ductus and help widen area of aortic constriction

A

PGE1

178
Q

Spectrum of undergrowth of left side of heart, including severe coarctation of aorta, severe aortic or mitral valve stenosis or atresia, hypoplasia of LV and ascending aorta. Coronary blood flow is retrograde from PDA

A

hypoplastic left heart syndrome (HLHS)

179
Q

what presents with Poor myocardial function, no systemic cardiac output once PDA closes andsevere CHF and shock

A

HLHS

**in utero diagnosis becoming more common

180
Q

treatments of HLHS

A 
-prior to repair, use PGE1 or PDA stent to keep DA open
or 
-Staged repair (Norwood operation)
-Heart transplantation
-Comfort care (hospice)
181
Q

Congestive heart failure (severe) with impaired alveolar ventilation and O2 diffusion causes

A

cyanosis from CHD

182
Q

4 elements of TOF

A
  1. Ventricular septal defect
  2. Overriding of ascending aorta
  3. Obstruction of RV outflow tract
  4. Right ventricular hypertrophy (muscle grows to overcome pressure)
183
Q

most common cyanotic congenital heart defect; may present beyond newborn period

A

tetralogy of fallot (TOF)

184
Q

treatment of TOF

A
  1. medical management of hypercyanotic episodes (“tet spells”) from transient increase in RV outflow tract obstruction)
    * *use propranolol (relax vessels to increase flow), oxygne, knee-chest position
  2. surgical repair when older
185
Q

a palliative shunt procedure is done (ie Blalock-Taussig) that connects subclavian artery to pulmonary artery
is done when

A

a baby is severely hypoxic in newborn period due to TOF

186
Q

The aorta & pulmonary a. arise from wrong sides

*2 closed systems

A

Transposition of the Great Arteries (TGA)

187
Q

treatment of TGA

A

create a PFO to allow blood flow to mix

188
Q

A single arterial vessel arises from the heart

Pulmonary vessels arise from the truncus

A

Truncus arteriososus

189
Q

What CHD ALWAYS has a large VSD present

A

Truncus arteriososus

190
Q

CHD Often associated with DiGeorge syndrome, a deletion of a portion of chromosome 12

A

Truncus arteriososus

191
Q
  • Pulmonary veins do not empty into left atrium

- Connection can be to right atrium, superior or inferior vena cava, coronary sinus

A

Total anomalous pulmonary venous return (TAPVR)

192
Q

Obstructed veins in TAPVR leads to

A

pulmonary venous hypertension, edema, and severe hypoxia

193
Q

treatment of TAPVR

A

surgical and emergic if obstructed

194
Q

What CHD requires an ASD for blood flow to get to left side of heart

A

TAPVR

195
Q

snowman heart on xray

A

TAPVR

196
Q

Tricuspid valve is absent

resulting in functionally hypoplastic right ventricle & pulmonary arteries

A

tricuspid atresia

197
Q

what presents with cyanosis and CHF

A

tricupsid atresia

198
Q

treatment of tricupsid atresia

A
  • PGE1 is initial therapy to maintain patent DA and VSD

- then surgery

199
Q

Prominent LV silhouette

Variable pulmonary blood flow on xray

A

tricupsid atresia

200
Q

Crucial in left-sided obstructive lesions & lesions with decreased pulmonary blood flow

A

PGE1

201
Q

what medication improves pulmonary edema

A

diuretics

202
Q

what medications improve cardiac contractility

A

Dopamine
dobutamine
digoxin

203
Q

cardiac caths are used to

A

open valves, atrial septum wiht balloon

204
Q

supplemental oxygen provides

A

increase pulmonary blood flow bc pO2 dilates pulmonary beds, alveolar oxygen delivery

Neonate (4 decks)

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